1. قال صلى الله عليه وسلم: )لا يلج النار من صلى قبل طلوع الشمس وقبل غروبها) رواه مسلم و قال صلى الله عليه وسلم : (من صلى الفجر في جماعة فهو في ذمة الله) رواه مسلم

2. Dr Jamal Naim PhD in Orthodontics Pre-clinical Periodontics Defense mechanisms of the periodontium (cont.)

3. Gingival Crevicular Fluid (GCF)  Source: capillary network under the junctional epithelium.  Exits capillaries, passes through connective tissue, across basement membrane, & between the large intercellular spaces of the JE. blood vessels in gingiva Tooth surface

4. Gingival blood supply

5. Gingival Crevicular Fluid (GCF) Methods of collection:  Absorbing paper strips (intra- or extrasulcular)  Twisted threads  Micropipettes  Intrasulcular washings

6. Gingival Crevicular Fluid (GCF) Amount: 0.1 mg in 3 minutes on periopaper (1.5 wide and 1mm inserted intrasulcular)

7. Gingival Crevicular Fluid (GCF) Increase of GCF amount by:  inflammation  mechanical stimulation: 1.Mastication of coarse food 2.Toothbrushing 3.Gingival massage  Smoking  Circadian periodicity  Hormones (contraceptives, ovulation and pregnancy)

8. Composition:  non-inflammatory fluid & a few cells from blood vessels  Contains non-clotting components of blood and a few PMN, antibodies.  Constituents of GCF important in the maintenance of JE function GCF in gingival health??????

10. Exudates as part of the inflammatory response usually contains:  Cellular elements (leukocytes, bacteria, desq. Epithelial cells)  Electrolytes such as calcium, sodium and potassium.  Organic compounds: proteins and carbohydrates Note that the GCF glucose level is 3 to 4 time higher than blood glucose level GCF in gingivitis

11.  Increased GCF flow is the very first sign of gingivitis; contributes to host defence by flushing bacterial colonies and their metabolites away from the tissues.  The very large mix of enzymes, cytokines etc in the GCF affect the functioning of the JE. GCF in gingivitis

12. GCF is usually not observed clinically Healthy no gingivitis gingivitis GCF in gingivitis

13.  PMN activity & performance,  Measure enzyme concentration (bacterial & host enzymes),  Collagen & proteoglycan breakdown products.  Measure level of antibodies to plaque bacteria  Bone breakdown products?????? Potential uses of GCF in periodontal diagnosis

14. GCF will ultimately provide information about current ACTIVITY of periodontal diseases; A simple ‘Dip stick’ test would be very useful. Potential uses of GCF in periodontal diagnosis

15.  GCF is a complex biochemical mix of both host & bacterial substances.  Most markers so far give information about gingivitis, not periodontitis.  We need a marker in GCF that is specific for BONE breakdown. Potential uses of GCF in periodontal diagnosis

16. Specific immune response Specific immune response can occur as an adaptation to protracted Chronic inflammation. It requires: T- lymphocytes (cellular immunity) and B-lymphocyte (humoral immunity) to generate the response. 4 phases of action (the pathway of adaptation): 1. Clonal selection 2. Clonal expansion 3. Clonal contraction 4. memory

17. Specific immune response T-lymphocyte: (cellular immunity) Are active also intracellular (e. g. antiviral) B-lymphocyte: Are active only extracellular Produce 9 isotypes of immunoglobulin (by primary response variable IgM) By secondary response (after differentiation to plasma cells) produce specific Ig's

18. Microbial virulence factors Periodontal disease is initiated and sustained by: bacteria and Bacterial products of the subgingival biofilm The virulence factors are: Factors that enable bacteria to colonize (Adherence) and invade host tissues (against the bathing effect of GCF) Factors that enable bacteria to cause tissue damage

19. Microbial virulence factors Surfaces ready for adherence are: root surfaces Soft tissues and preexisting calculus The presence of the acquired pellicle is essential for the adherence of first layers on the tooth (e. g. actinmyces viscosus) The adherence on calculus is made through coaggregation (different strains such as s. sanguis on a.viscosus)

20. Microbial virulence factors The invasion of host tissue give the germs the possibility to directly act beneath tissue that will be damaged (conective tissue and bone) The germs invade the tissues through ulcerations in the sulcus or directly through JE. Bacterial species that directly invade the soft tissues: actinomyces actinomycetem comitans Prevotella gingivalis Fusobacterium nucleatum Treponema denticola

21. Microbial virulence factors To survive bacteria must neutralize or evade different host defense mechanisms: Some examples: Adherence against bathing effect of saliva or GCF Leukotoxins of A. actinomycetem comitans (in aggressive P.) cause: Neutralization of PNM functions Killing of mature T- and B-lymphocyte Decreasing of response to antigens through suppression

22. Microbial virulence factors To treat periodontal diseases where bacteria invade the tissue can be successful after mechanical debridement and antibiotic therapy to eliminate germs from tissues.

23. Microbial virulence factors Substances directly or indirectly cause damage to host cells and tissues are: Proteases: digesting collagen, elastin, fibronectin, fibrin Leukotoxin: kill leukocytes LPS (endotoxins): damage tissues Other may activate inflammatory or cellular and humoral immune systems which secondarily damage the periodontium.

25. Cardinal signs of an inflammation In the classical description of inflammation an area is presented which appears macroscopically: Erethyma (redness) Edema (swollen) heat pain loss of function

26. Histopathological features of gingival inflammation In 1976, Page and Schroeder classified the progression of gingival and periodontal inflammation on the basis of the then available clinical and histopathological evidence. They divided the progressing lesion into four stages: The initial lesion The early lesion The established lesion The advanced lesion

27. I. The initial lesion Within 24h Clinical: invisible Histological: as a reaction histamine release dilation in the micro- vascular plexus beneath the JE (histamine release) and increase in the permeability of the micro-vascular bed fluids and proteins exude into the tissues Increase GCF Bacteria and their products may be flashed from the sulcus.

28. I. The initial lesion The intensity of host response determine whether the initial lesion resolves or evolves into a chronic inflammation

29. II. The early lesion clinical signs: After 1 week of plaque accumulation signs of gingivitis (erythema) appear because of more dilatation of the blood vessels and increase in its number at the surface. Bleeding on Probing may be evident Increased fluid exudation

30. II. The early lesion Histological: Increase in leukocyte migration PMNs, lymphocytes are predominated + very few plasma cells fibroblastic cytotoxic degeneration Collagen destruction occurs in the infiltrated area (main affected groups are the circular and dentogingival group) The basal cells of the JE+ SE have now proliferate to enhance the innate barrier to plaque

31. III. The established lesion After 2-3 weeks of accum. Of calculus Clinically: Increased fluid exudation more swelling Histological: Congestion of blood vessels with impaired venous return Gingival anoexemia (bluish color), and breakdown of hemoglobin in the connective tissue (deep redness) leukocyte migration More collagen loss JE is no longer closely attached to the tooth surface and the pocket epithelium has now formed

32. The established lesion reflected the histopathology of more chronic gingivitis Two types of established lesion One remains stable (not progressing) One becomes more active and converts to a progressive and destructive advanced lesion. III. The established lesion

33. Also known as periodontal breakdown reflect the progression of gingivitis to periodontitis. The pocket deepens, thus anaerobic ecological niche. Alveolar bone loss occurs. Fiber damage is extensive. JE migrates apically from the CEJ Plasma cells are dominated IV. The advanced lesion